Theories of cognition, emotion and the social world - missing links in psychosis

The conclusion is that there ceases to be room for expla-nations of the schizophrenic experience in terms of social contexts, and that cognitive accounts represent understanding at a dif

Theories of cognition, emotion and the social world: missing links in psychosis

Paul Bebbington, David Fowler, Philippa Garety, Daniel Freeman and Elizabeth Kuipers

Introduction

Throughout the twentieth century, clinicians and researchers struggled to establish

a convincing account of psychosis and the processes and mechanisms underlying its manifestations This effort depended on refinements of classification and case definition over the whole course of the century However, despite the huge invest-ment of intellectual energy and monetary resources, results have been slow in coming and disappointingly piecemeal It has become clear that psychosis is a phenomenon of great complexity Recent social and cognitive models of psychosis are attempts to deal with some aspects of this complexity We will argue for the appositeness of such models, and place them within the broader research effort in psychosis Before doing this, we need to revisit some of the consequences of the formulation of the concept of schizophrenia, the disorder that represents the core

of psychotic phenomena

A failed category?

The idea that schizophrenia is a failed category emerges regularly in the psychiatric and psychological literature, the most prominent current advocate being Bentall (2003) This is essentially a criticism of approaching schizophrenia as a medical entity The medical strategy of investigation involves the identification of syn-dromes, which, in turn, form the basis of theories These include those relating to aetiology, pathology, outcome and treatment (Wing, 1978) Syndromes are essen-tially theoretical constructs: while they can be regarded as disease entities, they are never really more than tentative Nevertheless, there is a tendency in psychiatry to

Society and Psychosis, ed Craig Morgan, Kwame McKenzie and Paul Fearon Published by Cambridge University Press # Cambridge University Press 2008.

regard psychiatric syndromes as having more virtue than they actually possess They do, however, form a useful basis for research If theories about syndromes are refuted, consideration may be given to abandoning them In medicine we generally reject theories, of aetiology and so on, before rejecting the theoretical construct represented by the syndrome We may nevertheless eventually decide that the syndrome has failed, in the sense that the knowledge built up in relation to it is confused and imprecise, and there may be better ways of organising the clinical information for the purposes of research There is current debate about whether

we have reached this stage with schizophrenia

One of the difficulties for a biomedical approach in psychiatry is the sheer cussedness of the subject matter It is, for example, extremely difficult to construct

a classification, as categories in psychiatry are notorious for overlapping one another This is not merely a problem of imprecise definition: the subject matter

is actually hierarchical rather than planar, and any attempt to construct a flat classification is thus probably doomed to failure

The nature of psychiatric phenomena creates three crucial problems for the definition of categories like schizophrenia The first is the threshold problem, that

is, the point at which the syndrome becomes recognisable and distinguishable from normal experience The second is the boundary problem, the difficulty of drawing valid lines between, for example, schizophrenia and bipolar disorder Added to this is a third problem, which is both empirical and conceptual This is that the disorder seems to be inherently difficult to explain

One of the early authorities to grasp the problem of the threshold was Jaspers (1913) He saw schizophrenia as the battleground between opposing traditions of explanation in science The methods of the physical sciences were concerned with causal explanation, whereas social sciences involved appreciation through a pro-cess of understanding, through meaningful connections His view was that where understanding failed (as it seems to in people’s attempts to share the experiences

of those deemed to be mad), we are left only with resort to physical explanation The implication is that in such circumstances we are facing a physical illness with physical causes The conclusion is that there ceases to be room for expla-nations of the schizophrenic experience in terms of social contexts, and that cognitive accounts represent understanding at a different level from biological explanations The resulting biological hegemony held sway in psychiatry until the last decades of the twentieth century, and is only now being replaced by a more flexible and comprehensive approach to the problems besetting scientific research

in schizophrenia

Jaspers himself never regarded schizophrenia as a no-go area for social and psychological research He was quite happy with the idea that psychosis could be meaningfully connected to circumstances, although reluctant to see the process

as wholly understandable He did acknowledge that it was difficult to identify the point at which paranoia became delusional, and there is now considerable evi-dence confirming his view

Psychosis as a continuum with normal experience

Modern cognitive models of psychosis actually start by postulating continuities between psychosis and normal experience The emergence of psychotic phenom-ena thus reflects an abnormal concatphenom-enation of largely normal mechanisms What

is weakness in the medical category, in this theoretical formulation becomes strength In the past, the urge to make a categorical distinction between psychosis and normality almost certainly led to a Procrustean tendency to discount unusual beliefs and experiences in people we would be reluctant to see as undergoing a psychosis However, it became apparent by the late 1980s that paranoid ideation and anomalous experiences, such as hearing voices, were not confined to clinical groups It is clear that the frequency of auditory hallucinosis greatly exceeds the accepted prevalence of psychosis (e.g., Wiles et al., 2006) The distinguishing feature of those in contact with services is the level of distress occasioned by their unusual experiences (Hanssen et al., 2003; van Os et al., 1999)

The distribution of unusual beliefs in the populace is also extensive Many people are convinced of the truth of ideas that are not supported by available and accessible evidence These include beliefs in astrology, alien beings, telepathy

or ghosts Political beliefs are held with strong conviction even though they may be untried, or indeed tried and found wanting People who hold these cherished ideas typically have a confirmatory bias, being unlikely to consider alternatives impar-tially These beliefs shade into what would be regarded as delusional, since the thinking that underpins them is similar in style to that in people with acknowl-edged psychosis

Attempts have been made to define delusions in terms that would enable them

to be distinguished clearly and reliably from normal thinking The form of words varies, but generally implies the following: they are held with a basic and compel-ling subjective conviction; they are not susceptible to contrary experience or to counter-argument; they are impossible, incredible or false; they lie outside the belief systems characteristic of the individual’s cultural group However, because

of the overlap with ‘normal’ thinking, it has been impossible to construct criteria that are, individually or jointly, both necessary and sufficient for an operational-ised definition (Bebbington and Broome, 2004)

The continua of beliefs in the community have been demonstrated empirically One example concerns ‘paranoid’ beliefs, in other words, those relating to self-reference and threat Freeman et al (2005b) found that 30% of an internet sample

of students had such ideas Moreover, the frequency distribution of individual paranoid ideas followed an exponential curve (Figure 14.1), with the relationship between them being non-hierarchical, such that more extreme ideas were predic-tive of those that were less extreme but not vice versa This finding has now been corroborated using general population data (Bebbington, P E et al The paranoia dimension in the general population (submitted to the British Journal of Psychiatry)) The pattern is much like that shown by affective symptoms (Melzer

et al., 2002; Sturt, 1981) At a single point in time the continuum is defined by differences between individuals, who are thus located at individual positions on the curve However, people are themselves likely to vary in a way that would place them at different positions on the curve at different times, dependent on changing circumstances In a sense, they would move along the curve

These findings have considerable relevance to the aetiology of psychosis They imply that in some people movement along a continuum (indeed probably more than one continuum) results in the emergence of psychosis Thus the role of aetiology is to explain exactly why particular people make this journey at particular times in their lives In the genetic arena, this suggests a focus on quantitative analyses (Linney et al., 2003), along with the identification of quantitative trait loci (Plomin et al., 1994) In the psychological domain, it implies the concatenation of different psychological attributes, some cognitive, some emotional (Hanssen et al.,

30

25

20

15

10

5

0

Total number of paranoia ideas

y = 24.474e –0.2569x

Figure 14.1 Distribution of paranoia scores in a student population (taken with permission from Freeman

et al., 2005b)

2005; Krabbendam and van Os, 2005; Krabbendam et al., 2005) There are also implications for treatment, in particular psychological treatments, such as cogni-tive behaviour therapy (Kuipers et al., 2006)

The boundary problem

The boundary problem, whereby schizophrenia is imprecisely separated from other psychiatric conditions, has also been a source of discomfiture The relation-ship between bipolar disorder and schizophrenia, for instance, is certainly ambig-uous Clearly some individuals have mood dysregulation, and some have psychotic experiences However, many have both, and in varying proportions While attempts may be made to see affective psychosis and non-affective psychosis as distinct, they really represent opposite ends of a spectrum, and this is reflected in considerable overlap in the candidate genes associated with the two conditions (Craddock and Owen, 2005; Craddock et al., 2005; 2006)

Mood disturbances of some kind are almost invariable in cases of schizophrenia Thus, up to 40% of people with schizophrenia also have clinical levels of depres-sion (Birchwood, 2003; Sands and Harrow, 1999), 30% meet criteria for post-traumatic stress disorder (Mueser et al., 1998), 20% have panic disorder (Turnbull and Bebbington, 2001) and up to 25%, obsessive compulsive disorder (Berman

et al., 1995) For a classification seeking to distinguish affective and non-affective forms of psychosis, this is an embarrassment However, once we cease to worry about the overlap and think of emotional changes as potentially an integral part of the psychotic process, it becomes possible to see it as a doorway to explanation This is easy for cognitive models of psychosis, which all involve an acknowledged role for affect (Birchwood, 2003; Garety et al., 2001)

Aetiological processes

What then of the problems of explaining schizophrenia in biomedical terms? We define schizophrenia in relation to people’s reports of their unusual mental experiences It would make life much simpler if we had privileged access to some underlying condition or entity However, all we have to go on is the disorder as defined, the phenomena, not the noumena In other words, it is the strange beliefs, the hallucinations, and their contents, that we have to explain

There has long been a prima facie assumption about aetiological theories in psychosis, a reductionist position placing genetic explanations at the beginning of the aetiological process Virtually all genetic research in schizophrenia has been based on the assumption that genetic abnormalities lead to abnormalities in protein function, with consequent distortions of enzymatic activity, and that

these in turn lead to corresponding deficits in neuronal function These deficits then result in cognitive dysfunctions that form the substrate for the schizophrenic experiences that permit the diagnosis of the disorder This is obviously a very useful working paradigm, but it must be treated with caution

The high heritability of schizophrenia is easy to demonstrate from twin studies (Craddock et al., 2005) However, recent research has served to emphasise that not only is schizophrenia a complex disorder to the clinical observer, it is also complex

in genetic terms Such disorders have relatively high population prevalence, are non-Mendelian and are imprecisely distinguished from the normal range The search for genes linked to schizophrenia has been long, arduous and expensive (Norton et al., 2006; Owen et al., 2005) Candidates have been unearthed, but their association with schizophrenia remains tentative The genes encoding dysbindin (DTNBP1) and neuroregulin (NRG1) are the strongest contenders, with evidence for other genes (disrupted in schizophrenia (DISC1), D-aminoacid oxidase activator (DAOA), regulator of G-protein signalling 4 (RGS4) and V-AKT murine thymoma viral oncogene homolog 1 (AKT1)) being at least suggestive (Norton et al., 2006) Some have been associated with abnormalities of brain structure and enzyme function, which, albeit plausible, would seem to have a tenuous connection to the schizophrenic phenotype (Callicott et al., 2005; Harrison and Weinberger, 2005; Meyer-Lindenberg et al., 2005) Given the modern synthesis of evolutionary theory, genetics and developmental biology, focusing solely on encoding for enzymes is likely to prove simplistic, even though links with schizophrenia may

be found After all, only two percent or so of the DNA in human cells produce proteins that act as enzymes, while much more is involved in complex regulatory systems that switch the functions of protein-encoding genes on and off, something clearly of potential relevance to an acknowledged developmental disorder like schizophrenia These issues have at last started to inform genetic research in schizophrenia (Glaser et al., 2006; Law et al., 2006; Lipska et al., 2006)

Adjacent elements in the aetiological process seem likely to fall far short of a one-to-one relationship, with the implication that at every step on the way the specificity of relationships is progressively lost The consequence is that the association of individual genes with schizophrenia must inevitably be attenuated, with small effect sizes (Norton et al., 2006)

Moreover, the genes identified so far seem to be associated with neurocognitive deficits (Hariri et al., 2003; Meyer-Lindenberg et al., 2005) These are plausible antecedents of negative symptoms of schizophrenia, and there is appreciable empirical support for the association between them (Pinkham et al., 2003) Thus genetic explanations so far lean towards an explanation of negative symptoms However, the heritability of schizophrenia is the heritability of positive symptoms, since it is from these that the condition is identified The potential association of

the Val/Val allelic form of COMT with vulnerability to psychotic responses to cannabis might be one way round this difficulty (Caspi et al., 2005) However, we fall far short of a comprehensive explanation in genetic terms for the positive symptoms responsible for the heritability of the condition in the first place There are further problems with the aetiological process The implicit unidir-ectionality is an act of faith that almost certainly cannot be sustained Thus the way

in which heritability is calculated means that it actually includes gene–environment interaction Moreover, gene–environment interaction covers environmental gene induction, and the inducing environment may be social as well as physical Thus, natural variation in the competency of mouse mothers affects their offspring’s responses to stress in later life (Meaney, 2001), apparently mediated by epigenetic changes involving histone regulation of DNA expression This is then maintained, and affects the offspring’s own parenting behaviour (Fish et al., 2004; Weaver

et al., 2004) Thus the causal direction may sometimes run from the social to the physical, rather than the other way around Furthermore, our knowledge about putative aetiological factors is based on induction Thus, because some people with schizophrenia have, for example, a family history of the same condition, an inductive leap is made to the conclusion that all schizophrenia has a genetic basis The frailty of the logic underpinning this inference is apparent As the same caveat applies to social theories, aetiological modesty is imperative on all sides The final problem relates to the nature of schizophrenic symptoms themselves Most of the experiences that form the basis of the identified symptoms of schizo-phrenia are about something: they carry within them representations of the social world (paranoid ideation is an obvious example of this) This is the characteristic

of intentionality identified by Brentano (1874) Defining a medical condition in terms of experiences that have intentionality means that explanations in purely physical terms will always be incomplete

This is the context in which models of psychosis involving social, emotional and cognitive elements have been developed They do not deny an important role for the physical matrix of disorder, but they do add to the complexity and probably to the potential of explanation They form one part of the overall model There are several variants, and all are better described as social-cognitive-emotional models They focus on the sorts of explanation that can be developed for considering the person with psychosis as an agent in a social and societal context They also seek to explain psychosis by trying to explain single symptoms or coherent groups of symptoms

Analysing single symptoms

The study of single psychotic symptoms, or single types of symptom, is assisted by

a clear account of the symptoms themselves Thus cognitive models encourage a

return to the precision of the early psychopathologists However, descriptions are amplified by attempts to discern processes that may underlie the mental experi-ences corresponding to the symptoms This activity should be distinguished from actual explanation – it is more akin to exegesis, and increases the potential targets for explanation An example of exegesis is provided by Frith in his persuasive account of passivity experiences as a combination of ‘forward memory’ and an exaggerated sense of agency (‘if it is not me, it must be someone else’) (Frith, 2005) Phenomenological analyses may also clarify linkages between symptoms conven-tionally regarded as separate For example, there are relationships between thought insertion, loud thoughts and thought broadcast The essence of thought insertion is not the idea of external origin, but the loss of the sense of possession of the mental experience This is shared by other passivity experiences, but also by auditory hallucinations Loud thoughts are thoughts acknowledged by the person experienc-ing them, but they have the quality of loudness shared by our experience of sound waves In this, they of course resemble auditory hallucinosis Thought broadcast has been described imprecisely, but close attention to the self-reports of those who suffer from it reveals that the essential feature is the experience of thoughts that are externally projected Such thoughts share this feature with some but not all forms

of auditory hallucinosis Thus these four types of symptoms exhibit variously the loss

of the sense of possession, loudness and external projection, and the exact pattern of these three features determines what symptoms may be identified

Projection and loudness merit further comment, as both can be seen as dis-tortions of normal processes It is probably of enormous evolutionary advantage to integrate the brain changes initiated by the immediate environment into an externally projected world This capacity for projection is self-evidently inherent

in human beings, and the external projection that characterises hallucination, thought broadcast and passivity experiences is thus also a failure of a normal mechanism Loudness is the mental experience normally attached to the brain events corresponding to the impact of sound waves on the cochlea As such, it flags

up these events as relating to the external world When the flag becomes attached

to other mental experiences, they become anomalous (as in loud thoughts) Loudness and external projection may have a very similar neural embodiment, but their separation in particular psychotic symptoms suggests they are distinct

A further example of this kind of analysis concerns the issue of meaning This can

be interpreted as an emotional component of mental experience In psychiatric disorder, levels of meaning can be either increased or reduced, or both The most obvious example of this reregulation occurs in depression and mania People with depression lose a sense of meaning, just as those with mania acquire it Perception carries an emotional charge that becomes apparent when it is lost Loss of meaning underlies experiences such as dulled perception, depersonalisation and derealisation,

while in mania heightened perception affects the perceived intensity of colours and sounds and the beauty of music However, meaning also attaches to non-perceptual mental experiences In depression, this includes lost emotions: a painful sense of knowing and remembering the emotion but no longer being able to feel it In general, reduction in the emotional component of mental experiences is negative if not always painful, while increases are more ambiguous Thus, the increased signification attached to paranoid ideas is distressing while that attached to heightened perception and to some forms of ideas of reference may be pleasurable Capgras’ syndrome is a form of delusional depersonalisation, whereby the loss of the emotional component

of person recognition results in delusional ideas concerning the replacement of known people by unknown impostors In contrast, the Fregoli syndrome is associated with an increased signification of person perception, resulting in the belief that strangers are actually friends and relatives in disguise It is also possible to conceive

of mental experiences involving loss of the sense of possession as being down-regulations of the emotional significance of the experience

There is, thus, a prima facie argument for suggesting that change in the emo-tional components of mental experience underlies many psychiatric symptoms including those involved in psychosis This would again imply continuities between symptoms regarded as psychotic and those that are not It remains possible, of course, that this proposition arises from over-interpretation and that there is no underlying commonality of the type described

The distinctiveness of symptoms probably implies that there are also distinctions between the processes that generate them Thus disorders like Fregoli and Capgras may include a specific malfunction of the part of the fusiform gyrus concerned with facial recognition (Pinkham et al., 2005) Nevertheless, the possibility of a common contribution has been acknowledged by Kapur (2003) in his proposition that dopamine dysfunction in psychosis often increases salience but sometimes reduces it

Cognitive models of psychosis

Over the last 10 years or so, several cognitive models of psychosis have been proposed (e.g., Bentall et al., 2001; Birchwood, 2003; Broome et al., 2005; Fowler, 2000; Freeman et al., 2002; Garety et al., 2001; Morrison, 2001) They seek to identify the origins of psychosis by explaining the causation of individual symptoms To do this, they adduce interactions between social contexts, emo-tional tone and cognitive processing They vary in the emphasis laid on these components and the extent to which the involved processes are regarded as unusual concatenations of normal internal and external circumstances

Our own model emphasises the continuity of psychotic and non-psychotic experiences; a central role of appraisal; the role of low self-esteem and emotional

changes; and findings relating to adverse social environments While we do not specify biological explanations in the model, they are implicit In other words, some of the components may be related to abnormal neural function The model emphasises, as one route to symptom development, the significance of cognitive dysfunction leading to anomalous experiences, and the appraisal of these experi-ences as externally caused Unlike Morrison (2001), we think this distinguishes psychosis from common mental disorders, such as anxiety and depression Virtual reality experiments with normal subjects are of interest here Some normal sub-jects develop persecutory thoughts even in neutral scenarios Crucially, it seems that previous anomalous experiences of a schizotypal variety differentiate between people who are merely anxious in the situation and those who develop persecutory ideas (Freeman et al., 2003, 2005a)

A considerable amount of recent work has tested hypotheses derived from these cognitive models We ourselves start from the common assumption that people who develop a psychotic illness do so on the basis of a predisposition of biological or social origin that renders them vulnerable to stress This vulnerability is expressed in emotional and cognitive changes that contribute to anomalies of conscious experi-ence, of which the most salient example is auditory hallucinosis Anomalous expe-riences seem likely to be embodied in information processing disturbances (Frith, 1992; Gray et al., 1991; Hemsley, 1993, 2005) These authors have suggested that anomalous experiences are intrusions into conscious awareness arising from defects

in the continuous integration of current experience with stored memories However, the mere experience of anomalies does not lead to overt psychosis without an interpretation that lends them personal significance and attributes to them an external origin Such interpretation is shaped by information processing biases, pre-existing schematic beliefs about the self and others, and emotional disturbance, all of which interact with (and sometimes originate from) the social contexts that individuals find themselves in We will consider these elements in further detail

Social influences on psychosis

Psychosocial factors are comprehended in a variety of ways Research into the relationship between life events and various psychiatric conditions has been a major thrust in psychiatry over the past 40 years Life events obviously range from the catastrophic to the relatively banal, and events of all types have been studied in relation to schizophrenia Initial investigations involved recent events with significant social connotations (Bebbington et al., 1996) More recent research has examined the ebb and flow of daily hassles (see Chapter 9)

Other research has involved quite complex aspects of the person’s environment, for example, the immediate family environment (see Chapter 8) and social